ライフサイエンスコーパス: excitable cell

1 ng variation can be applied to models of any excitable cell.

2 responses that resemble action potentials in excitable cells.

3 on and propagation of electrical impulses in excitable cells.

4 protein underlying the membrane potential in excitable cells.

5 lectrical signals to biological responses in excitable cells.

6 cal for chemical and electrical signaling in excitable cells.

7 els are crucial for electrical signalling in excitable cells.

8 propagates action potentials in electrically excitable cells.

9 action potentials in nerve, muscle and other excitable cells.

10 t in the amplification of Ca(2+) influx into excitable cells.

11 hibitory effect of many neurotransmitters on excitable cells.

12 o quickly recycle vesicle proteins in highly excitable cells.

13 se intracellular Ca(2+) concentration in non-excitable cells.

14 tial for initiating action potentials within excitable cells.

15 of fundamental activities in other kinds of excitable cells.

16 al, thereby enabling electrical signaling in excitable cells.

17 ng subthreshold oscillations in electrically excitable cells.

18 tion of discrete downstream responses in non-excitable cells.

19 ls, transporters, and signaling molecules in excitable cells.

20 on potentials during electrical signaling in excitable cells.

21 between VGSC activity and gene expression in excitable cells.

22 iological voltages and calcium levels in non-excitable cells.

23 re not physiological conditions for most non-excitable cells.

24 gated Ca(2+) channels controls activities of excitable cells.

25 er membrane-associated proteins found within excitable cells.

26 ion and conduction of electrical impulses in excitable cells.

27 nist-induced cytosolic Ca(2+) signals in non-excitable cells.

28 second messengers in both excitable and non-excitable cells.

29 s the main pathway for Ca(2+) extrusion from excitable cells.

30 tif conferring membrane targeting in primary excitable cells.

31 n of other ion channels in neurons and other excitable cells.

32 in a functional context, in neurons or other excitable cells.

33 ed in modulating the electrical responses of excitable cells.

34 elation to SOC channels in excitable and non-excitable cells.

35 initiate and propagate action potentials in excitable cells.

36 eceptors expressed in the plasma membrane of excitable cells.

37 in cellular Ca2+ to fundamental responses in excitable cells.

38 n-B targets ion channels and transporters in excitable cells.

39 of action potential firing frequency in many excitable cells.

40 ibitory effects of many neurotransmitters on excitable cells.

41 Ca(2+) channels including Ca(v)1.3 in other excitable cells.

42 ce shapes the complex electrical response of excitable cells.

43 ys a critical role in Ca2+ signalling in non-excitable cells.

44 stimulation approaches to optical control of excitable cells.

45 nnels to the function and differentiation of excitable cells.

46 tion and propagation of action potentials in excitable cells.

47 intenance of specialized membrane domains in excitable cells.

48 ium channels (Cav) mediate calcium influx in excitable cells.

49 K+ leak (K2P) pores that control activity of excitable cells.

50 ting electrical impulses in nerves and other excitable cells.

51 about how this process might be modulated in excitable cells.

52 overed role in electrical synchronization of excitable cells.

53 t least two complementary modes of action on excitable cells.

54 r the electrophysiological behaviour of many excitable cells.

55 a role for control of membrane potential of excitable cells.

56 way responsible for diverse functions in non-excitable cells.

57 channels) are involved in repolarization of excitable cells.

58 als in nerve, muscle, and other electrically excitable cells.

59 signal transduction elements in electrically excitable cells.

60 ng in signaling in taste receptors and other excitable cells.

61 cation current (Ih) is widely distributed in excitable cells.

62 ant determinants of firing frequency in many excitable cells.

63 ) initiate the action potential waveforms in excitable cells.

64 rucial for the normal electrical activity of excitable cells.

65 ar communication in astrocytes and other non-excitable cells.

66 d to encode SOCCs responsible for CCE in non-excitable cells.

67 l signal transduction in nearby electrically excitable cells.

68 nels play important functional roles in many excitable cells.

69 change that propagates along the membrane of excitable cells.

70 orses of spike generation and propagation in excitable cells.

71 ical forces regulate membrane traffic in non-excitable cells.

72 how Ca2+ channels regulate the physiology of excitable cells.

73 axiK channel expression in non-excitable and excitable cells.

74 a diverse array of cellular functions within excitable cells.

75 e electrical signalling in neurons and other excitable cells.

76 entry and downstream signal transduction in excitable cells.

77 cellular function in both excitable and non-excitable cells.

78 ly act as a fluorescent activity reporter in excitable cells.

79 e quantification of calcium responses in non-excitable cells.

80 cally important events in the development of excitable cells.

81 facilitate voltage-sensitive Ca(2+) entry in excitable cells.

82 xpression characteristics of Kv1 channels in excitable cells.

83 membrane potential in both excitable and non-excitable cells.

84 ion channels have been clearly identified in excitable cells.

85 hich follows the stimulation of a variety of excitable cells.

86 e-dependent Ca2+ currents, characteristic of excitable cells.

87 distinct functions in both excitable and non-excitable cells.

88 sodium channels (Navs) play crucial roles in excitable cells.

89 ls which leads to physiological signaling in excitable cells.

90 nels widely employed for photostimulation of excitable cells.

91 e primary mechanism for mCa(2+) extrusion in excitable cells.

92 Calcium Entry (SOCE) is well studied in non-excitable cells.

93 rrents and TRPM8-mediated calcium signals in excitable cells.

94 and frequency of action-potential firing in excitable cells.

95 l players in many physiological processes in excitable cells.

96 nderstanding of the role of Kv11 currents in excitable cells.

97 tic changes and the electrical properties of excitable cells.

98 nnels often overlaps in neurons and in other excitable cells.

99 eatly enhances their functional diversity in excitable cells.

100 ing signal transduction in neurons and other excitable cells.

101 of action potentials is commonly observed in excitable cells.

102 als in nerve, muscle, and other electrically excitable cells.

103 um (K(+)) channel desirable for silencing of excitable cells.

104 for optogenetic stimulation of electrically excitable cells.

105 ght control of resting membrane potential in excitable cells.

106 s a novel regulator of cell processes in non-excitable cells.

107 critical for proper electrical signaling in excitable cells.

108 rize the voltage dynamics of large groups of excitable cells.

109 tion and propagation of action potentials in excitable cells.

110 Nav) channels propagate action potentials in excitable cells.

111 annel activity to gene expression changes in excitable cells.

112 trigger or modify action potentials (APs) in excitable cells.

113 maintenance of resting membrane potential in excitable cells.

114 ials is important to understand electrically-excitable cells.

115 iming mechanisms across different systems of excitable cells.

116 rol the upstroke of the action potentials in excitable cells.

117 In cardiac myocytes, as in most excitable cells, action potential propagation depends es

118 l cellular process particularly important in excitable cell activities such as hearing.

119 applications in analyzing the regulation of excitable cell activity in genetically tractable organis

120 In non-excitable cells, agonist-induced depletion of intracellu

121 maintain high input resistance in these non-excitable cells also requires the K(+) channel subunits

122 Our results indicate that excitable cells and animal behavior can provide modulato

123 ) channels initiate electrical signalling in excitable cells and are the molecular targets for drugs

124 The extent to which excitable cells and behavior modulate animal development

125 annels (Kv) are responsible for repolarizing excitable cells and can be heavily glycosylated.

126 concentration dynamics in a general class of excitable cells and cell assemblies of concentric cylind

127 teins in biology, regulating the activity of excitable cells and changing in diseases.

128 data previously reported for SK3 channels in excitable cells and hepatocytes.

129 the predominant Ca(2+) influx pathway in non-excitable cells and is activated in response to depletio

130 channel Orai regulates Ca(2+) entry into non-excitable cells and is required for proper immune functi

131 In humans, ICG labels excitable cells and is routinely visualized transdermall

132 t as the negative resistance of electrically excitable cells and of tunnel diodes can be embedded in

133 (BK-type) channels, abundantly distribute in excitable cells and often localize to the proximity of v

134 roteins that generate an action potential in excitable cells and play an essential role in neuronal s

135 se results demonstrate that Merkel cells are excitable cells and suggest that they release neurotrans

136 e for understanding electrical signalling in excitable cells and the actions of drugs used for pain,

137 contribute to the subthreshold properties of excitable cells and thereby influence behaviors such as

138 urthermore, we demonstrate that biosynthetic excitable cells and tissues can repair large conduction

139 er for extracellular electrical recording of excitable cells and tissues thus providing a valid alter

140 nnels are fundamental signaling molecules in excitable cells, and are molecular targets for local ane

141 ns, genes that function in multiple types of excitable cells, and genes in the signaling pathway of t

142 esting membrane voltage in many electrically excitable cells, and heritable mutations cause periodic

143 requenin) are expressed at highest levels in excitable cells, and some of them regulate desensitizati

144 vascular smooth muscle tissue, electrically excitable cells, and some tumors.

145 tion potential activity across many types of excitable cells, and the activity of L-, N-, P/Q- and R-

146 rofound impact on the electrical behavior of excitable cells, and the regulation of this property cou

147 the upstroke of the action potential in most excitable cells, and their fast inactivation is essentia

148 ping the input-output profiles of individual excitable cells, and therefore the activity of neuronal

149 mbrane proteins that play essential roles in excitable cells, and they are key targets for antiepilep

150 can yield [Ca(2+)](Cyt) oscillations in non-excitable cells, and, under certain conditions, the ER-m

151 l muscle with Ca(2+) entry mechanisms in non-excitable cells are also reviewed.

152 Given that excitable cells are arranged in interconnected networks,

153 Electrically excitable cells are important in the normal functioning

154 ds used to assess the electrical activity of excitable cells are often limited by their poor spatial

155 Agonist-activated Ca(2+) signals in non-excitable cells are profoundly influenced by calcium ent

156 Since the Ca2+ dynamics inside the excitable cells are spatiotemporal while the membrane vo

157 ost of hair cells, as well as those of other excitable cells, are still immature.

158 ral patterns of resting potentials among non-excitable cells as instructive cues in embryogenesis, re

159 nd their relation to the normal functions of excitable cells as well as pathophysiology.

160 hannels are fundamental to the physiology of excitable cells because they underlie the generation and

161 These results indicate that regulation of excitable cell behavior by neurotransmitter-mediated mod

162 m channels (K(Na)), suggested to function in excitable cells both during physiological conditions and

163 ium-release-activated current (ICRAC) in non-excitable cells but at present there is little informati

164 ts in the generation of action potentials in excitable cells, but despite numerous structure-function

165 a variety of functions in neurons and other excitable cells, but excessive calcium influx through th

166 NCX) is a critical calcium efflux pathway in excitable cells, but little is known regarding its auton

167 els is essential for electrical signaling in excitable cells, but the structural basis for voltage se

168 suppression of high-frequency discharges of excitable cells by local anesthetics (LA) is largely det

169 ion flux and generate electrical signals in excitable cells by opening and closing pore gates.

170 In many non-excitable cells Ca2+ influx is mainly controlled by the

171 ltage-regulated Ca2+ channels whereas in non-excitable cells Ca2+ influx is mediated by store-operate

172 er increase or decrease in calcium influx in excitable cells can be associated with BD.

173 model to simulate calcium transients in non-excitable cells (consisting of a plasma membrane Ca2+ pu

174 ClC proteins regulate membrane potential of excitable cells, contribute to epithelial transport, and

175 Collectively LOTUS-V extends the scope of excitable cell control and simultaneous voltage phenotyp

176 Data and simulations suggested that excitable cells could use differences in K(+) channel gl

177 ctrophysiology beyond canonical electrically excitable cells could yield exciting new findings.

178 for activation of CICR by Ca2+ influx in non-excitable cells, demonstrate a previously unrecognized r

179 sfunction in these pathways results in human excitable cell disease.

180 Potassium (K(+)) exits electrically excitable cells during normal and pathophysiological act

181 nd light-sensitive ion currents operating in excitable cells, e.g. cardiomyocytes or neurons.

182 expressed in electrically excitable and non-excitable cells, either as alpha-subunit (BKalpha) tetra

183 Excitable cells express a variety of ion channels that a

184 Many excitable cells express L-type Ca(2+) channels (LTCCs),

185 en used in vertebrate systems to investigate excitable cell firing and calcium transients, but both t

186 hannels, CaV, regulate Ca(2+) homeostasis in excitable cells following plasma membrane depolarization

187 e activation of channelrhodopsin 2 (ChR2) in excitable cells for the first time to our knowledge.

188 In electrically non-excitable cells, for example epithelial cells, this is a

189 Whether nonexcitable cells may modulate excitable cell function or even contribute to AP conduct

190 s an important but potentially toxic role in excitable cell function.

191 Ion channels in excitable cells function in macromolecular complexes in

192 ssing questions central to understanding how excitable cells function.

193 Electrically excitable cells harness voltage-coupled calcium influx t

194 The G protein-coupled receptors in excitable cells have prominent roles in controlling Ca2+

195 nt of intracellular Ca(2+) signaling in many excitable cells; however, the role of this mechanism in

196 tration of localized chemical stimulation of excitable cells illustrates the potential of this techno

197 istently, cell-specific ablation of dopamine-excitable cells in dorsal, but not ventral, striatum inh

198 versely, optogenetic stimulation of dopamine-excitable cells in dorsal, but not ventral, striatum sub

199 gnals can be used to control the function of excitable cells in intact tissues or organisms.

200 nnels mediate synaptic communication between excitable cells in mammals.

201 oral dynamics induced by any neuron or other excitable cells in the animal.

202 ODs) by reshaping the electric discharges of excitable cells in the periphery.

203 urrounding myocytes, suggesting that the non-excitable cells in the scar closely follow myocyte actio

204 es in physiological processes, especially in excitable cells, in which they shape the action potentia

205 hannel function and SOCE in a variety of non-excitable cells including lymphocytes and other immune c

206 igand-gated cation channels, present on many excitable cells including vas deferens smooth muscle cel

207 niques to follow the activation state of non-excitable cells, including lymphocytes.

208 the rising phase of the action potential in excitable cells, including neurons and skeletal and card

209 tol trisphosphate (IP(3)) stimulation of non-excitable cells, including vascular endothelial cells, c

210 to determine the mechanism through which non-excitable cells influence the spontaneous activity of mu

211 For example, in excitable cells inwardly rectifying potassium (GIRK) cha

212 In excitable cells, ion channels are frequently challenged

213 signaling by homomeric P2XRs expressed in an excitable cell is subtype-specific, which provides an ef

214 Calcium entry into excitable cells is an important physiological signal, su

215 is unique to neurons or also occurs in other excitable cells is currently unknown.

216 that cortactin-mediated actin remodeling in excitable cells is not only important for cell structure

217 Exocytosis in excitable cells is strongly coupled to Ca2+ entry throug

218 cally regulates the flow of sodium ions into excitable cells, is a common functional consequence of i

219 neration of Ca2+i signals, especially in non-excitable cells, is store-operated Ca2+ entry (SOCE).

220 erences can limit the translational value of excitable cells isolated from model organisms.

221 In many excitable cells, KATP channels respond to intracellular

222 In non-excitable cells, KCNQ1 forms a complex with KCNE3, which

223 CaV1 function and suggests a means by which excitable cells may dynamically tune CaV activity.

224 ponse to voltage changes across electrically excitable cell membranes.

225 d may play a fundamental role in controlling excitable cell metabolic regulation.

226 to modulate the plasma membrane potential of excitable cells, mitochondria have thus far eluded optog

227 ts suggest that electrically integrated, non-excitable cells modulate the excitability of cardiac pac

228 differences between cardiomyocytes and other excitable cells modulate vulnerability to conduction fai

229 To signal properly, excitable cells must establish and maintain the correct

230 The excitable cells of Dictyostelium discoideum show traveli

231 trol the upstroke of the action potential in excitable cells of nerve and muscle tissue, making them

232 t drives action potential generation in many excitable cells of the brain, heart, and nervous system.

233 t signaling pathways control the activity of excitable cells of the nervous system and heart, and are

234 tosolic free Ca2+ concentration ([Ca2+]i) in excitable cells often acts as a negative feedback signal

235 In addition, unlike in excitable cells, our data suggest a minimal physiologica

236 t voltage-gated Ca(2+) entry, which typifies excitable cells, overwhelms the effect of any capacitati

237 questration mechanisms to various aspects of excitable cell physiology are incompletely understood.

238 fic plasma membrane domains is necessary for excitable cell physiology.

239 In many species, excitable cells preserve their physiological properties

240 In excitable cells, receptor-induced Ca(2+) release from in

241 sequences of such activity in the setting of excitable cells remains the central focus of much of the

242 iggering CICR, and indicate that CICR in non-excitable cells resembles CICR in cardiac myocytes with

243 Alterations in K(v)7-mediated currents in excitable cells result in several diseased conditions.

244 Opening of Na(+) channels in excitable cells results in influx of Na(+) and cellular

245 d synaptic patterning, as well as aspects of excitable cell signal transduction and neuromodulation.

246 In excitable cells, small-conductance Ca2+-activated potass

247 ecules subserving transmembrane signaling of excitable cells; special emphasis is placed here on prot

248 ole Ca2+ entry mechanism in a variety of non-excitable cells, store-operated calcium (SOC) influx is

249 In non-excitable cells stromal interaction molecule 1 (STIM1) i

250 They also are expressed in non-excitable cells such as macrophages and neoplastic cells

251 um channels initiate electrical signaling in excitable cells such as muscle and neurons.

252 Ca2+ channels, previously known to exist in excitable cells such as neurons and muscle cells, are sh

253 high frequency oscillating magnetic field on excitable cells such as neurons are well established.

254 an important role in electrical signaling of excitable cells such as neurons, cardiac myocytes, and v

255 nd viability impairment in aggregate-exposed excitable cells such as peripheral neurons and cardiomyo

256 mparable with those found in compartments of excitable cells such as the postsynaptic density and jux

257 eau bursting is typical of many electrically excitable cells, such as endocrine cells that secrete ho

258 Electrically excitable cells, such as neurons, exhibit tremendous div

259 aracterization of several other types of non-excitable cells, such as the microglia (brain macrophage

260 oduce and analyse a simple model for two non-excitable cells that are dynamically coupled by a gap ju

261 erkel cells are genetically programmed to be excitable cells that may participate in touch reception,

262 Corticotrophs are excitable cells that receive input from two hypothalamic

263 Corticotrophs are excitable cells that receive input from two hypothalamic

264 In the case of ion channels in excitable cells, the dynamics of signaling to the nucleu

265 As in other excitable cells, the ion channels of sensory receptors p

266 In excitable cells, the main mediators of sodium conductanc

267 In non-excitable cells, the major Ca2+ entry pathway is the sto

268 In many non-excitable cells, the predominant mode of agonist-activat

269 hannels are important in the heart and other excitable cells, there are virtually no specific drugs f

270 In excitable cells these channels are composed of the ion-f

271 In non-excitable cells, thiol-oxidizing agents have been shown

272 nnels fine-tunes the electrical signaling in excitable cells through an internal timing mechanism tha

273 current inhibition that is widely present in excitable cells through modulation of ion channels by sp

274 ulation of K(+) channel inactivation enables excitable cells to adjust action potential firing.

275 late action potentials into Ca(2+) influx in excitable cells to control essential biological processe

276 ycosylation of ion channels could be used by excitable cells to modify cell signaling.

277 brane potential and regulate the response of excitable cells to various stimuli.

278 + signalling in the rat megakaryocyte, a non-excitable cell type in which membrane potential can mark

279 as investigated in rat megakaryocytes, a non-excitable cell type recently shown to exhibit depolarisa

280 local Ca(2+) ion signalling in a variety of excitable cell types.

281 v) channels at sites of function in multiple excitable cell types.

282 ying transient outward K(+) currents in many excitable cell types.

283 ribute to the afterhyperpolarization in many excitable cell types.

284 eld of agonist-activated Ca(2+) entry in non-excitable cells underwent a revolution some 5 years ago

285 dulating the firing patterns of electrically-excitable cells using surface plasmon resonance phenomen

286 es significant thermally mediated effects on excitable cells via basic thermodynamic mechanisms that

287 In excitable cells, voltage-gated calcium channels (Cav) ar

288 In excitable cells, voltage-gated calcium influx provides a

289 In excitable cells, voltage-gated sodium (Na(V)) channels a

290 Indeed, when the ratio of intrinsically excitable cells was increased or decreased, the number o

291 the restricted expression of scn1ba mRNA in excitable cells, we detected scn1bb transcripts and prot

292 ant role in propagating action potentials in excitable cells, we have identified a novel role in rege

293 channels (SK channels) have been reported in excitable cells, where they aid in integrating changes i

294 how these enzymes are regulated by Ca(2+) in excitable cells, where they predominate.

295 cs (LAs) block voltage-gated Na+ channels in excitable cells, whereas batrachotoxin (BTX) keeps these

296 d play a physiological role, particularly in excitable cells, which can generate large transients in

297 Ventricular myocytes are excitable cells whose voltage threshold for action poten

298 ding for proteins modulating the membrane of excitable cells, whose biological correlates are assesse

299 ctivate different regions of ChR2-sensitized excitable cells with high spatial resolution.

300 een resting V(mem) and the physiology of non-excitable cells with implications in diverse areas, incl